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      Does Maturity Affect Cephalic Perfusion and T/QRS Ratio during Prolonged Umbilical Cord Occlusion in Fetal Sheep?

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          Abstract

          T/QRS ratio monitoring is used to help identify fetal asphyxia. However, immature animals have greater capacity to maintain blood pressure during severe asphyxia, raising the possibility that they may show an attenuated T/QRS increase during asphyxia. Chronically instrumented fetal sheep at 0.6 of gestation (0.6 GA; n = 12), 0.7 GA ( n = 12), and 0.8 GA ( n = 8) underwent complete umbilical cord occlusion for 30 min, 25 min, or 15 min, respectively. Cord occlusion was associated with progressive metabolic acidosis and initial hypertension followed by severe hypotension, with a more rapid fall in mean arterial blood pressure (MAP) and carotid blood flow (CaBF) with advancing gestation. T/QRS ratio rose after occlusion more rapidly at 0.8 GA than in immature fetuses, to a similar final peak at all ages, followed by a progressive fall that was slower at 0.8 GA than in the immature fetuses. The increase in T/QRS ratio correlated with initial hypertension at 0.8 GA ( P < 0.05, R 2 = 0.38), and conversely, its fall correlated closely with falling MAP in all gestational groups ( P < 0.01, R 2 = 0.67). In conclusion, elevation of the T/QRS ratio is an index of onset of severe asphyxia in the last third of gestation, but not of fetal compromise.

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          Neuropsychological and educational problems at school age associated with neonatal encephalopathy.

          Adverse cognitive and educational outcomes are often ascribed to perinatal hypoxia without good evidence. To investigate neurocognitive and behavioural outcomes after neonatal encephalopathy. Sixty five children with neonatal encephalopathy, identified using the Trent Neonatal Survey database for 1992-1994, were followed up at the age of 7 years. They were examined at school, with a classmate for those in mainstream school, by a paediatrician and a psychologist. Neonatal encephalopathy was graded as moderate or severe using published definitions. Fifteen children had major disability, all with cerebral palsy; eight were in special school with severe cognitive impairment (IQ<55). Disability was present in 6% of the moderate and 42% of the severe encephalopathy group. Of the 50 children without motor disability, cognitive scores were lowest in the severe group (mean IQ difference from peers -11.3 points (95% confidence interval (CI) -19.0 to -3.6) and with similar scores for the moderate group compared with classmates (mean difference -1.7 points (95% CI -7.3 to +3.9). Neuropsychological testing showed similar findings in all domains. In particular, memory and attention/executive functions were impaired in the severe group. Despite relatively small differences in performance of the moderate group, special educational needs were identified more often in both encephalopathy groups, associated with lower achievement on national curriculum attainment targets. After neonatal encephalopathy, subtle cognitive impairments are found in the absence of neuromotor impairment. Subtle impairments are found more commonly after a more severe clinical course. Studies of brain protection strategies require long term follow up to study effects on cognitive outcome.
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            Afferent and efferent components of the cardiovascular reflex responses to acute hypoxia in term fetal sheep.

            1. We studied the effects of acute isocapnic hypoxia on arterial and central venous pressures, carotid and femoral blood flows and heart rate in intact and carotid denervated fetal sheep between 118 and 125 days gestation, after pre-treatment with either saline, atropine or phentolamine. Electrocortical activity (ECoG) and the incidence of fetal breathing movements (FBM) were also compared between intact and carotid denervated fetuses. 2. There were no significant differences between intact and denervated fetuses in any variable measured during normoxia. Soon after the onset of hypoxia a marked bradycardia occurred in intact, but not in denervated fetuses. Femoral blood flow and femoral vascular resistance (perfusion pressure/femoral blood flow) increased in intact, but not in denervated fetuses. Carotid blood flow increased in both groups of fetuses during hypoxia, but carotid vascular resistance did not change. During hypoxia, the incidence of FBM and low-voltage ECoG was similarly reduced in both groups of fetuses. 3. Atropine produced a rise in fetal heart rate during the control period in intact but not in denervated fetuses. At the onset of hypoxia atropine prevented the initial bradycardia seen in intact fetuses. In denervated fetuses a further increase in heart rate occurred throughout the hypoxia. 4. All denervated fetuses treated with phentolamine died during the hypoxic challenge, but nine out of fourteen intact fetuses treated with phentolamine survived. 5. In intact fetuses which survived hypoxia after treatment with phentolamine, the increase in arterial blood pressure was smaller and the increase in femoral resistance did not occur. In these fetuses a rise in heart rate occurred in hypoxia. Carotid vascular resistance decreased during hypoxia after administration of phentolamine. 6. Our results indicate that the initial cardiovascular responses of the late gestation sheep fetus to hypoxia are reflex, and that the carotid chemoreceptors provide the afferent limb of this reflex. The bradycardia is mediated through a muscarinic pathway, as it is blocked by atropine. The femoral vasoconstriction is mediated through an alpha-adrenergic mechanism, mediated both neurally by a carotid chemoreflex and via catecholamines released directly from the adrenal medulla. Both these components are blocked by phentolamine. 7. The differences in survival between intact and denervated fetuses during hypoxia after phentolamine suggest that the carotid chemoreflex response to hypoxia involves mechanisms in addition to vagal efferents to the heart and alpha-adrenergic actions at peripheral blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)
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              GLYCOGEN RFSERVES AND THEIR CHANGES AT BIRTH AND IN ANOXIA

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                Author and article information

                Journal
                Obstet Gynecol Int
                Obstet Gynecol Int
                OGI
                Obstetrics and Gynecology International
                Hindawi Publishing Corporation
                1687-9589
                1687-9597
                2014
                16 February 2014
                : 2014
                : 314159
                Affiliations
                Fetal Physiology and Neuroscience Group, Department of Physiology, University of Auckland, Auckland 1023, New Zealand
                Author notes

                Academic Editor: Richard Berger

                Author information
                http://orcid.org/0000-0002-6053-2864
                http://orcid.org/0000-0002-6374-9372
                Article
                10.1155/2014/314159
                3945773
                943e6fcd-1666-4390-b434-1dd4a41fb75a
                Copyright © 2014 Guido Wassink et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 20 September 2013
                : 18 December 2013
                : 31 December 2013
                Categories
                Research Article

                Obstetrics & Gynecology
                Obstetrics & Gynecology

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